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PubMed2005

Glycosaminoglycans mediate invasion and survival of Enterococcus faecalis into macrophages.

Enterococcus faecalis is responsible for a large variety of nosocomial infections. The intestinal barrier is thought to be one of the preferential portals of entry of enterococci, and the ability of E. faecalis to survive within peritoneal macrophages may contribute to spreading to distant sites. We examined the ability of a polysaccharide-expressing (biofilm-positive) E. faecalis strain and an isogenic biofilm-negative mutant to enter and survive within professional and nonprofessional phagocytes. Biofilm-positive bacteria survived longer in all cell systems than did biofilm-negative bacteria, through a process of receptor-mediated endocytosis that is dependent on functional reorganization of microtubules and polymerization of microfilament and on activation of protein kinases but not ATPases or protein phosphatases. We suggest that glycosaminoglycans--specifically heparin, heparan sulfate, and chondroitin sulfate A--are the host receptors for enterococci on professional and, possibly, nonprofessional phagocytes, allowing entry of enterococci into cell compartments where killing mechanisms are inhibited.

Animals↗
PubMed2005

Identification of BCRP as transporter of benzo[a]pyrene conjugates metabolically formed in Caco-2 cells and its induction by Ah-receptor agonists.

Breast cancer resistance protein (BCRP/ABCG2) is known to actively transport various anticancer drugs and to restrict the uptake of the food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine from the gut lumen. The present study reveals that BCRP is involved in the transport of phase-2 metabolites of the carcinogen benzo[a]pyrene (BP) in the human intestinal cell line Caco-2. Treatment with the selective BCRP inhibitor Ko 143 (5 microM) inhibited the apical transport of BP-3-sulfate (BP3S) to 83% of control levels in TC7 cells and to 64% of control levels in Caco-2 cells. The apical transport of BP-3-glucuronide was inhibited by Ko 143 to 76% of control levels in TC7 cells. Furthermore, the expression of BCRP is most likely aryl hydrocarbon receptor (AhR) dependent, as treatment of Caco-2 cells with known AhR agonists including 2,3,7,8-tetrachlorodibenzo-p-dioxin, BP, indolo[3,2-b]carbazole and benzo[k]fluoranthene increased both mRNA and protein levels of BCRP. Induced BCRP protein was found to be functionally active, since pre-treatment of TC7 cells with oltipraz, indolo[3,2-b]carbazole or benzo[k]fluoranthene increased the amount of apically transported BP3S to as much as 180% of that in the controls. The induction of BCRP (mRNA and protein expression) by indolo[3,2-b]carbazole was inhibited in Caco-2 cells by co-incubation with the AhR antagonist PD98059 (2'-amino-3'-methoxyflavone). In summary, this study provides strong evidence that BCRP is an important part of the intestinal barrier protecting the body from food-associated contaminants such as the carcinogen BP.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2005

The importance of the gastrointestinal system in the pathogenesis of heart failure.

Chronic heart failure (CHF) is a multi-organ disease with increasing evidence for the involvement of the gastrointestinal (GI) system in this syndrome. In recent research, the gut has received very little attention from cardiologists as its role in the pathogenesis of cardiovascular disease is poorly understood. Intestinal ischaemia may play an important role in bacterial translocation by increasing bowel permeability. Decreased cardiac function can reduce bowel perfusion and so clearly impairs the function of the intestinal barrier. There is an increasing evidence to suggest that a 'leaky' bowel wall may lead to translocation of bacteria and/or endotoxin, which may be an important stimulus for inflammatory cytokine activation in CHF. Impaired functioning of the GI system may also contribute to malnutrition and cachexia in CHF. It is hoped that by improving our understanding of the role of the gut in cardiac disease will lead to the development of novel therapeutic strategies in the future.

Bacterial Translocation↗
PubMed2001

Smectite in the treatment of acute diarrhea: a nationwide randomized controlled study of the Italian Society of Pediatric Gastroenterology and Hepatology (SIGEP) in collaboration with primary care pediatricians. SIGEP Study Group for Smectite in Acute Diarrhea.

BACKGROUND: Childhood gastroenteritis is associated with considerable health costs. The natural clay dioctahedral smectite increases intestinal barrier function and is effective against infectious diarrhea in children in developing countries. The purpose of this work was to investigate the efficacy of smectite in Italian children with acute diarrhea of mild to moderate severity. METHODS: A national, prospective, randomized, case-controlled study was performed in collaboration with primary care pediatricians. Children seen by pediatricians for acute gastroenteritis were treated with oral rehydration solution (ORS) alone or ORS with smectite. Parents returned a form in which total duration of diarrhea, incidence of vomiting and fever, persistence of diarrhea for more than 7 days and hospital admissions were recorded. RESULTS: Eight hundred four children with acute diarrhea were randomly assigned to treated or control groups. Administration of smectite was associated with significant reduction of the duration of diarrhea, as judged by stool frequency and consistency. The incidence and duration of vomiting and fever were not different. Diarrhea lasted more than 7 days in 10% of treated and in 18% of control children (P < 0.01). Hospital admission was necessary in seven treated and six control children. No side effects were observed. CONCLUSIONS: Smectite reduces the duration of diarrhea and prevents a prolonged course. It may therefore consistently reduce the costs of gastroenteritis.

Acute Disease↗
PubMed2001

Bacterial [correction of baterial] translocation in humans.

Bacterial translocation is a phenomenon in which live bacteria cross the intestinal barrier. The definition may be broadened to include transmural passage of bacterial cell wall components such as lipopolysaccharide and peptidoglycan polysaccharide. After translocation, bacteria or their products reach the mesenteric lymph nodes. From there, it is possible that enteric bacteria, their cell wall components, or both may disseminate throughout the body, causing sepsis, shock, multisystem organ dysfunction, or death of the host. Bacterial translocation and its complications have been shown clearly to occur in animal models, but its existence and importance in humans has been difficult to ascertain. The purpose of this review is to evaluate the data from studies in humans on the occurrence of bacterial translocation and, more importantly, to evaluate its role as a cause of death in humans. Studies from trauma and intensive care centers often imply that bacterial translocation is a major contributor to sepsis, shock, and multisystem organ failure in humans. However, the data reviewed herein do not support that view clearly. Carefully designed studies are needed to determine the relevance of bacterial translocation in human disease.

Animals↗
PubMed1990

Splenectomy influences endotoxin-induced bacterial translocation.

To determine whether splenectomy affects the antibacterial defenses of the gut, experiments were performed using bacterial translocation (BT) as a marker of intestinal barrier failure. The incidence of BT was measured 8 days after splenectomy or sham-splenectomy in mice receiving or not receiving endotoxin (0.1 mg IP). Splenectomy does not appear to promote BT from the gut, since the incidence of bacterial translocation after splenectomy or sham-splenectomy (5%) were not different. A second experiment was performed to determine whether the resistance to endotoxin-induced BT was modified after splenectomy. The incidence of endotoxin-induced BT was 73% in the unoperated control group, 59% in the sham-splenectomy group, but 23% in the splenectomy group (p less than 0.002). Thus, splenectomy but not sham-splenectomy increased the resistance of otherwise healthy mice to endotoxin-induced BT.

Animals↗
PubMed1998

Is early enteral nutrition in acute pancreatitis dangerous? About 20 patients fed by an endoscopically placed nasogastrojejunal tube.

Bowel rest during treatment of acute pancreatitis deprives the gut of nutrients and affects its structure and function. Enteral feeding is usually performed late in the course of acute pancreatitis and therefore cannot prevent intestinal barrier dysfunction and possible bacterial translocation. To assess the effect of early enteral nutrition we performed a prospective study on 21 patients (11 males/10 females) presenting with severe acute pancreatitis (13 biliary, 6 alcoholic, and 2 miscellaneous). Severity was established by a mean Ranson score of 3.57. All but one patient could be fed through a double-lumen nasogastrojejunal tube within 60 h after admission. No significant complication of the technique was observed. We conclude that early jejunal feeding can be used safely in severe acute pancreatitis. Further comparative studies are necessary to demonstrate any superiority to total parenteral nutrition.

Acute Disease↗
PubMed2005

Food components and immune function.

PURPOSE OF REVIEW: Enhancing immune function or alternatively dampening inflammatory processes by specific food components has received a lot of interest. The purpose of this review is to summarize recent findings with the emphasis on underlying mechanisms. RECENT FINDINGS: Dietary beta-glucans are relatively new candidates in the field of immune modulation by diet. In-vitro and animal studies suggest that beta-glucans shift inflammatory profiles to a Th1 type, which may enhance resistance against bacterial and parasitic infections. Regarding polyunsaturated fatty acids, there is evidence that n-3 fatty acids from fish oils (eicosapentaenoic acid and docosahexaenoic acid) dampen inflammatory responses. Whether eicosapentaenoic acid or docosahexaenoic acid is responsible for this phenomenon remains controversial. It is also inconclusive whether the plant-derived n-3 fatty acid alpha-linolenic acid has the same antiinflammatory effects as observed for fish oils. Saturated fatty acids may activate toll-like receptors and consequently the inflammatory pathway. The effect of total fat intake is controversial, since high-fat diets have been found to suppress immune function, while also improving intestinal barrier function. Finally, Gingko biloba was found to lower nuclear factor kappaB and activator protein 1 activation, possibly due to its high content of polyphenols. SUMMARY: In this review we discuss the nutritional components able to enhance immune function or show antiinflammatory effects. It can be concluded that diet certainly has the potential to direct immune responses. Apart from studies on fish oils, however, evidence from human studies is limited.

Animals↗
PubMed2002

Management of Lithuanian children's acute diarrhoea with Gastrolit solution and dioctahedral smectite.

OBJECTIVE: Acute gastroenteritis represents a major cause of morbidity and mortality worldwide among children, and rehydration treatment has been one of the cornerstones in the management strategy. The natural clay dioctahedral smectite (Smecta) increases intestinal barrier function and is effective against infectious diarrhoea in children. The purpose of this work was to compare the efficacy and tolerance of Lithuanian children's diarrhoea treatment with dioctahedral smectite combined with hypotonic oral rehydration solution (ORS)--Gastrolit--versus Gastrolit alone to establish the influence of Smecta on serum electrolyte balance in young children with diarrhoea and mild or moderate dehydration. METHODS: Smecta combined with ORS (study group) and ORS alone (control group) were evaluated in a multicentre, open, randomized trial in 54 children aged 6-48 months hospitalized for acute diarrhoea (mostly rotavirus aetiology) and signs of mild and moderate dehydration. The main outcomes examined were duration of diarrhoea, fever, number of vomiting episodes, and serum electrolyte balance before and after treatment. RESULTS: The mean duration of diarrhoea was significantly shorter in the study group (42.3 +/- 24.7 h) than in the control group (61.8 +/- 33.9 h). No side effects of Smecta were observed. The changes of sodium, potassium, chloride and calcium concentrations after treatment were minimal and in the normal range. CONCLUSIONS: Smecta significantly reduced the duration of diarrhoea, was safe and well tolerated, and had no impact on the adsorption of electrolytes. Smecta could be used together with ORS in children suffering from acute gastroenteritis (without uncontrollable vomiting) with mild and moderate dehydration.

Antidiarrheals↗
PubMed2003

The gesture life of high mobility group box 1.

PURPOSE OF REVIEW: Products of infection, ischemia, and injury stimulate the innate immune system to release proinflammatory cytokines, which act locally to activate specific cellular immune responses and initiate recovery. In pathological cases, however, cytokines are released systemically, resulting in progressive tissue injury, hypotension, organ dysfunction, or death. Observations that animals frequently succumb to systemic inflammation long after the peak activity of tumor necrosis factor and interleukin-1beta suggest that later-acting, downstream inflammatory factors can mediate the pathological sequelae of lethal systemic inflammation. Here, the authors review evidence that the chromosomal protein high mobility group box 1 is a late-acting, downstream mediator of pathological inflammation. RECENT FINDINGS: High mobility group box 1 recently has been identified as a proinflammatory cytokine with significantly delayed release kinetics, as compared with tumor necrosis factor and interleukin-1beta, in animal models of lethal systemic inflammation induced by endotoxin or peritonitis. Administration of exogenous high mobility group box 1 induces acute lung injury, intestinal barrier dysfunction, and lethal systemic inflammatory responses. Its functional cytokine domain has been mapped to the DNA-binding B box, providing structural information that may be useful in the rational design of new therapeutics that target the protein's activity. SUMMARY: Several high mobility group box 1 antagonists have recently been identified. These inhibitors may prove effective in a significantly wider therapeutic window than has been available for previous anti-cytokine strategies, because high mobility group box 1 appears in serum with a significantly delayed kinetics as compared with other cytokines.

Animals↗
PubMed2006

Systemic autoimmune disorders in celiac disease.

PURPOSE OF REVIEW: Celiac disease is an immune-mediated disorder clinically characterized by a multitude of symptoms and complications. The comorbidity between celiac disease and other autoimmune disorders has been clearly established. RECENT FINDINGS: Two main theories have been postulated to explain this comorbidity: (1) linkage disequilibrium between the genes responsible for celiac disease and those responsible for the coexpressed autoimmune diseases or (2) untreated celiac disease leading to the onset of other autoimmune diseases. This article reviews the current literature supporting either theory and places the current knowledge in the field within the context of the most recent data on the pathogenesis of celiac disease. SUMMARY: The current literature did not clearly establish which of the two theories explain the comorbidity between celiac disease and other autoimmune disorders. There is, however, growing evidence that the loss of the intestinal barrier function typical of celiac disease could be responsible of the onset of other autoimmune disease. This concept implies that the autoimmune response can be theoretically stopped and perhaps reversed if the interplay between autoimmune predisposing genes and trigger(s) is prevented or eliminated by a prompt diagnosis and treatment.

Animals↗
PubMed2007

Heat shock stress ameliorates cytokine mixture-induced permeability by downregulating the nitric oxide and signal transducer and activator of transcription pathways in Caco-2 cells.

Proinflammatory cytokines are known to impair intestinal barrier function and to activate signaling pathways, whereas heat shock responses prevent cytokine-induced mucosal damage. We hypothesized that heat shock response blocks the effects of proinflammatory cytokines by regulating nitric oxide (NO) production and the activities of the Janus kinase/signal transducer and activator of transcription (STAT) pathway. A monolayer of Caco-2 cells were pretreated with sodium arsenite (SA, 500 micromol/L) for 1 h, followed by a 1-h recovery, and then stimulated with a cytokine mixture (cytomix: tumor necrosis factor alpha [10 ng/mL], interferon beta [1000 U/mL], and interleukin [IL] 1beta [1 ng/mL]) for 24 h. The permeability of horseradish peroxidase and fluorescein isothiocyanate-conjugated Dextran and transepithelial resistance and potential difference were measured in Ussing chambers. Interleukin-6, IL-8, NO, inducible NO synthase mRNA, STAT activity, and suppressor of cytokine signaling (SOCS) expression were measured in medium or cell lysates. Cytomix resulted in increased epithelial permeability of both fluorescein isothiocyanate-conjugated Dextran and horseradish peroxidase; whereas treatment of Caco-2 cells with SA 500 micromol/L blocked the cytomix-induced permeability changes. In addition, SA treatment decreased cytomix-induced NO production and inducible NO synthase mRNA expression and decreased the levels of STAT1, STAT3, SOCS1, and SOCS3. The SA treatment also decreased cytomix-induced IL-6 and IL-8 production in a dose-dependent manner. In conclusion, cytomix increased epithelial permeability, which is associated with increased NO and STAT activities. The SA treatment ameliorated cytomix-induced permeability, possibly through the downregulation of the NO and Janus kinase/STAT pathways.

Caco-2 Cells↗
PubMed2003

The synergistic effects of hypoxia/reoxygenation or tissue acidosis and bacteria on intestinal epithelial cell apoptosis.

BACKGROUND: Clinical data indicate that gut perfusion deficits must be rectified within 24 hours after traumatic injury to decrease organ failure and death. Ischemia/reperfusion injury to the gut causes enterocyte apoptosis (Apo), which may contribute to intestinal barrier failure. The temporal response of enterocyte Apo to acidosis and hypoxia/reoxygenation (H/R) in vitro is unknown. The purpose of this study was to examine the effect of various time points of acidosis or H/R on enterocyte apoptosis and monolayer integrity in an in vitro model. METHODS: Caco-2 cell monolayers were made acidic (Dulbecco's modified Eagle's medium, pH 6.9) by hydrochloric acid or exposed to 95% nitrogen/5% carbon dioxide (hypoxia) and then 21% oxygen (reoxygenation). Escherichia coli C-25 were added to the apical media in subsets. Apo and necrosis were quantified by flow cytometry. Permeability was determined by fluorescein isothiocyanate-dextran. Transepithelial electrical resistance (TEER) indexed monolayer. RESULTS: Extracellular acidosis and C-25 significantly increased apoptosis of Caco-2 cells at 18 hours (extracellular acidosis [EC] + C-25, 14.5 +/- 3.0; control, 3.8 +/- 0.8; p < 0.001 by analysis of variance). Similarly, the H/R + C-25 group showed a significant increase in apoptosis at 12 hours (H/R + C-25 vs. control, 22.86 +/- 2.12 vs. 3.74 +/- 0.7; p < 0.001 by analysis of variance). The permeability difference was not significant for EC + C-25 versus control at 18 hours (0.68 +/- 0.25 vs. 0.43 +/- 0.0.0.36, respectively; p > 0.05). The H/R + C-25 group had a profound increase in permeability over control at 12 hours (10.8 +/- 0.5 vs. 2.1 +/- 0.3, respectively; p < 0.001). The TEER was significantly lowered for EC versus control at 18 hours (458 +/- 1.5 vs. 468 +/- 8.2) and at 0, 6, and 18 hours for EC + C-25 (409 +/- 28.1, 443 +/- 16.8, and 438 +/- 8.9 vs. 455 +/- 6.5, 467 +/- 6.5, and 469 +/- 8.2, respectively). There was no significant change in the H/R and H/R + C-25 groups. CONCLUSION: Synergism of H/R or tissue acidosis and bacteria caused increased Apo, TEER, and permeability in vitro.

Acidosis↗
PubMed2025

Systematic identification and characterization of regulators of aryl hydrocarbon receptor signaling.

The human aryl hydrocarbon receptor (AHR) integrates chemical signals derived from the environment, gut microbes, and endogenous sources to regulate processes ranging from intestinal barrier integrity to xenobiotic detoxification. Despite strong evidence that dysregulation of AHR signaling is a causal factor in metabolic and autoimmune disorders, we currently lack a comprehensive understanding of the factors that regulate AHR activity in human cells. Here, we use genome-scale CRISPR screening to systematically identify regulators of AHR signaling in hepatocytes. The resulting datasets recapitulate the core AHR signaling pathway and identify a large network of regulators. Many of these factors have roles beyond AHR signaling, reflecting that AHR signaling is deeply integrated into human cell biology. We further dissect this network to reveal novel modes of regulation of AHR expression, protein levels, and signaling. For example, we find that the E3 ubiquitin ligase UBR5 sustains AHR signaling by counteracting degradation of ligand-bound AHR. Finally, we identify components of the AHR regulatory network that are specific to cell types and ligands as potential nodes to manipulate AHR signaling in a targeted manner for therapeutic benefit. Overall, our results define the regulatory network that underpins AHR activation, with implications for our understanding of host-microbe interactions and integrative chemosensation and the etiology of metabolic and inflammatory disorders.

Journal Article↗
PubMed1982

Different role of secretory IgA in the pathogenesis of RAST-positive and RAST-negative atopic dermatitis.

Secretory-IgA (SIgA) concentrations were determined in whole saliva, unstimulated or stimulated by lemon juice, of thirty-eight children with atopic dermatitis, which comprised three adolescents, sixteen with IgE detected by RAST to one or more common allergen and twenty-two without specific IgE by RAST. There were thirty healthy controls matched for age and sex. The mean amount of total IgE was significantly greater in the RAST-positive than in the RAST-negative group. The mean SIgA concentration in unstimulated saliva of the RAST-positive atopic dermatitis group was less than that of the RAST-negative atopic dermatitis group and control groups, through the mean concentrations of SIgA of stimulated saliva were not significantly different in the three groups. It is suggested that the pathogenesis of atopic dermatitis may differ in children with or without specific-IgE antibodies; in those who were RAST-positive deficient exclusion of allergen by the intestinal barrier contributed to the pathogenesis, but not in those who were RAST-negative.

Adolescent↗
PubMed2004

Activator protein-1 signalling pathway and apoptosis are modulated by poly(ADP-ribose) polymerase-1 in experimental colitis.

Poly(ADP-ribose) polymerase-1 (PARP-1) is activated in response to DNA injury in the nucleus of eukaryotic cells and has been implicated in intestinal barrier dysfunction during inflammatory bowel diseases. In this study we investigated whether PARP-1 may regulate the inflammatory response of experimental colitis at the level of signal transduction mechanisms. Mice genetically deficient of PARP-1 (PARP-1(-/-)) and wild-type littermates were subjected to rectal instillation of trinitrobenzene sulphonic acid (TNBS). Signs of inflammation were monitored for 14 days. In wild-type mice, TNBS treatment resulted in colonic ulceration and marked apoptosis, which was associated with decreased colon content of the antiapoptotic protein Bcl-2, whereas the proapoptotic Bax was unchanged. Elevated levels of plasma nitrate/nitrite, metabolites of nitric oxide (NO), were also found. These inflammatory events were associated with activation of c-Jun-NH(2) terminal kinase (JNK), phosphorylation of c-Jun and activation of the nuclear transcription factor activator protein-1 (AP-1) in the colon. In contrast, PARP-1(-/-) mice exhibited a significant reduction of colon damage and apoptosis, which was associated with increased colonic expression of Bcl-2 and lower levels of plasma nitrate/nitrite when compared to wild-type mice. Amelioration of colon damage was associated with a significant reduction of the activation of JNK and reduction of the DNA binding of AP-1. The data indicate that PARP-1 exerts a pathological role in colitis possibly by regulating the early stress-related transcriptional response through a positive modulation of the AP-1 and JNK pathways.

Animals↗
PubMed2005

Degradation of the HilC and HilD regulator proteins by ATP-dependent Lon protease leads to downregulation of Salmonella pathogenicity island 1 gene expression.

Salmonella pathogenicity island 1 (SPI1) enables infecting Salmonella to cross the small intestinal barrier and to escape phagocytosis by inducing apoptosis. Several environmental signals and transcriptional regulators modulate the expression of hilA, which encodes a protein playing a central role in the regulatory hierarchy of SPI1 gene expression. We have previously shown that Lon, a stress-induced ATP-dependent protease, is a negative regulator of hilA, suggesting that it targets factors required for activating hilA expression. To elucidate the mechanisms by which Lon protease negatively regulates SPI1 transcription, we looked for its substrate proteins. We found that HilC and HilD, which are positive regulators of hilA expression, accumulate in Lon-depleted cells, and that the enhancement of SPI1 expression that occurs in a lon-disrupted mutant is not observed in the lon hilC hilD triple null mutant. Furthermore, we demonstrated that the half-lives of HilC and HilD are, respectively, about 12 times and three times longer in the Lon-depleted mutant, than in the Lon+ cells, suggesting that Lon targets both of HilC and HilD. In view of these findings, we suggest that the regulation of SPI1 expression is negatively controlled through degradation of the HilC and HilD transcriptional regulators by Lon.

Bacterial Proteins↗
PubMed2004

Enteropathogenic Escherichia coli EspF is targeted to mitochondria and is required to initiate the mitochondrial death pathway.

Enteropathogenic Escherichia coli (EPEC) is a causative agent of infant diarrhoea in developing countries. The EspF protein is the product of the espF gene found on the locus of enterocyte effacement, the key pathogenicity island carried by EPEC and enterohemorrhagic E. coli. EspF is injected from adherent EPEC into host cells via a type III secretion system and was previously shown to induce apoptotic cell death and to be required for disruption of host intestinal barrier function. In this work, we show by immunofluorescence and fractionation studies that EspF is targeted to host mitochondria. The N-terminal region of EspF serves as a mitochondrial import signal and, when expressed within cells, can target hybrid green fluorescent protein to mitochondria. Assessment of mitochondrial membrane potential in infected epithelial cells indicated that EspF plays a role in the mitochondrial membrane permeabilization induced by EPEC infection. Furthermore, EspF was associated with the release of cytochrome c from mitochondria into the cytoplasm and with caspase-9 and caspase-3 cleavage. These findings indicate a role for EspF in initiating the mitochondrial death pathway.

Caspase 3↗